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PubMed1983

Diagnosis and behavior of juvenile rhabdomyosarcoma.

The main problems in the diagnosis of rhabdomyosarcoma are 1) distinction of undifferentiated examples from other small cell malignancies, especially soft-tissue Ewing's tumor and lymphoma; 2) distinction of spindling examples from fibrosarcoma, leiomyosarcoma, malignant fibrous histiocytoma, polyhistioma, and other sarcomas; 3) recognition of minimal criteria on small samples such as needle biopsy specimens or frozen sections; and 4) recognition of rhabdomyosarcoma in uncommon sites such as bone (mandible), perineum, retroperitoneum, and chest. In 95 pediatric cases diagnosed and treated at Royal Alexandria Hospital for Children--45 after the introduction of combined therapy--minimal diagnostic criteria were assessed. Cross-striations were found in only one third of cases; longitudinal myofibrils were more common and more helpful. There was much overlap between histologic types, and the microscopic patterns had little bearing on prognoses in preadolescent children. Fourteen cases could not be further differentiated ("embryonal sarcoma, probably rhabdomyosarcoma")--nine small-cell tumors; four tumors from genitourinary tract or head for which very small biopsy specimens were available, and one spindling retroperitoneal neoplasm. In all, slight evidence suggested embryonal rhabdomyosarcoma; this evidence included oat-shaped nuclei and, in a few cells, deeply eosinophilic cytoplasm, small elongated processes, or myxoid or alveolar foci--features that exclude lymphoma and Ewing's tumor. In six cases that were originally classified as poorly differentiated or undifferentiated, later material confirmed the presence of rhabdomyosarcoma by showing a predominantly well-differentiated (pleomorphic) or alveolar pattern after therapy. In 14 remaining undifferentiated cases, immunoperoxidase staining with antihuman-myoglobin serum was positive in five. With combined therapy there was 100 per cent survival among patients with paratesticular, limb, and stage I and stage II tumors; considerably improved survival among patients with head and neck, pelvic, and stage III tumors; and 100 per cent mortality among patients with intra-abdominal and stage IV tumors.

Biopsy↗
PubMed2003

Fine-needle aspiration of synovial sarcoma: criteria for diagnosis: retrospective reexamination of 37 cases, including ancillary diagnostics. A Scandinavian Sarcoma Group study.

The cytologic criteria of synovial sarcoma in fine-needle aspirates were defined by a retrospective examination of 37 primary tumors. Irrespective of subtype, a typical pattern at low power was found, provided the yield was rich. The typical pattern was a mixture of dispersed cells with the presence of striped nuclei and cell-tight tumor tissue fragments with irregular borders. Often a branching network of vessels was present in the fragments, imitating a true vascular tumor. Except in poorly differentiated synovial sarcomas, the tumor cells were, small to medium in size, with rounded, ovoid, or fusiform bland nuclei with inconspicuous nucleoli. In the biphasic variant, small glandular- or acinar-like structures were present, although not in all cases. In the poorly differentiated type, however, the cellular pleomorphism was marked with the presence of cells with irregular nuclei and rhabdomyoblast-like cells, corresponding to the pleomorphic variant. The Ewing's sarcoma-like and the atypical spindle cell variants of poorly differentiated synovial sarcoma were not diagnosed in the material. An unequivocal diagnosis of sarcoma is possible when the yield is rich. However, ancillary diagnostics are necessary for a correct diagnosis, to avoid important pitfalls, such as other sarcomas with bland tumor cells and vessel-rich tumor fragments, in particular, solitary fibrous tumor and true hemangiopericytoma. Electron microscopic and/or molecular genetic analyses were better diagnostic adjuncts than immunocytochemistry.

Biopsy, Fine-Needle↗
PubMed1986

Hydrolytic cleavage of methotrexate gamma-polyglutamates by folylpolyglutamyl hydrolase derived from various tumors and normal tissues of the mouse.

Folylpolyglutamate hydrolase (folyl hydrolase) activity derived from murine tumors and various normal tissues was measured by means of high performance liquid chromatography using methotrexate polyglutamates as substrate. Enzyme-mediated hydrolysis was considerably greater (10-20-fold) on a specific activity basis in extracts from all normal mouse tissues (kidney greater than bone marrow greater than small intestine approximately equal to liver) than from tumor cells (Sarcoma 180 greater than Ehrlich approximately equal to L1210 cells). Enzyme preparations from purified absorptive and crypt cell epithelium from mouse small intestine exhibited comparable levels of specific activity and were greater than that derived from the total organ. Folyl hydrolase from mouse kidney showed mixed endo- and exopeptidase activity while that derived from all other normal tissues and tumor cells was consistent with endopeptidase activity. Levels of cell-free folyl hydrolase activity derived from tumor cells varied substantially with the phase of growth in vivo. Also, levels were appreciably lower from the same cells grown in vitro. Hydrolysis by crude or partially purified enzyme preparations from mouse small intestine or tumor cells conformed to Michaelis-Menten kinetics (single saturable component). Rates of hydrolysis and Km values were proportional to gamma-glutamyl chain length in the case of L1210 cell-derived enzyme but not for enzyme derived from small intestine. Km values derived for 4-amino-10-methylpteroyldiglutamate were the same [Km = 80.4 +/- 9 (SE) microM] for small intestine and L1210 cells. However, with 4-amino-10-methylpteroyltetraglutamate Km values were 3-fold lower for tumor cell preparations and 8-fold lower for preparations derived from small intestine. Fourfold lower Km values for 4-amino-10-methylpteroyldiglutamate were obtained with enzyme derived from Sarcoma 180 cells as compared to the enzyme from L1210 or intestinal cells. Varying levels of folyl hydrolase activity for methotrexate polyglutamates in cell-free preparations from different tumor cells appeared to reflect differences in in situ hydrolytic activity shown for the same substrate when internalized. The relevance of these results to antifolate pharmacology and, specifically, to a role for polyglutamates of 4-aminofolate compounds in determining cytotoxicity and selective antitumor activity of these agents is discussed.

Animals↗
PubMed1991

Paraspinal tumors: techniques and results of brachytherapy.

Because of their proximity to nerve roots and the spinal cord, it is frequently difficult to achieve complete resection of paraspinal tumors. We have used brachytherapy in an attempt to prevent local recurrence and its associated neurological sequelae. This report analyzes our experience with 35 patients to determine the feasibility, optimal techniques, and efficacy of this approach. The tumor types were non small-cell lung cancer (18), sarcomas (9), and other tumor types (8). Temporary, single plane implants using Ir-192 (median minimum peripheral dose 3000 cGy) were used in 21 patients, and permanent I-125 implants were used in 14 cases (median matched peripheral dose 12,500 cGy). Local control was achieved in 51% (18/35). However, local control was poor when lung cancers were implanted and in cases where the dura was exposed. Radiation myelitis did not occur despite the combined effects of previous external beam radiotherapy (N = 21) and brachytherapy. Our experience demonstrates that combined surgery and paraspinal brachytherapy can be performed with acceptable toxicity and is reasonably effective in preventing local relapse and its neurologic sequelae, particularly for tumors other than lung cancers.

Brachytherapy↗
PubMed1995

Translocation t(9;22)(q22;q12) is a primary cytogenetic abnormality in extraskeletal myxoid chondrosarcoma.

The cytogenetic and in vitro growth characteristics of 3 cases of extraskeletal myxoid chondrosarcoma (EMC) are described. In cell culture, the tumor cells retained the immunocytochemical and ultrastructural characteristics of EMC. Cytogenetically, 2 of the cases showed an apparently identical t(9;22)(q22;q12). In one case, the t(9;22) was found together with a dup(I)(q12q44), and in the other case it was found together with several other aberrations. The third case had an inv(10)(p11.2q22) as the sole karyotypic abnormality. Of 4 cases of EMC previously analyzed, 2 showed a t(9;22)(q22;q11-12) and one case of a t(9;22;15)(q31;q12.2;q25). Thus, 5 out of 7 cases of EMC showed recombination between 9q22-31 and 22q11-12, indicating that this represents a tumor specific abnormality. The breakpoints on 22q were in all 5 cases cytogenetically indistinguishable from those seen in Ewing's sarcoma with t(11;22), clear-cell sarcoma with t(12;22), and desmoplastic small round cell tumors with t(11;22). Molecular cloning of these translocation breakpoints revealed involvement of the EWS gene (located at 22q12) in all 3 tumor types. These observations raise the intriguing question of whether the EWS gene might also be involved in the t(9;22) in EMC.

Aged↗
PubMed1992

Chronic oral etoposide: trials at Indiana University and with the Hoosier Oncology Group.

Etoposide has proven to be an active agent in the treatment of a variety of neoplasms, particularly germ cell cancers and small cell lung cancer. Yet despite its widespread use, the optimal dose and schedule for etoposide remain unknown. The fact that its efficacy appears to be schedule dependent, along with the recent availability of an oral formulation, formed the basis for several trials at Indiana University and through the Hoosier Oncology Group. These trials evaluated chronic daily administration of the drug in several malignancies. In testicular cancer, etoposide was shown to have a possible role in adjuvant therapy for refractory disease or as part of combination chemotherapy. In small cell lung cancer, etoposide demonstrated activity in both previously treated and untreated patients. The drug, however, had little impact on patients with advanced non-small cell lung cancer, advanced melanoma, or advanced soft tissue sarcoma. Since etoposide appears to be most effective in refractory small cell lung cancer and germ cell tumors, we believe the drug should be explored in tumors with a known history of chemosensitivity to conventionally administered etoposide.

Administration, Oral↗
PubMedDate not supplied

A case of peripheral primitive neuroectodermal tumor of the ovary.

Peripheral primitive neuroectodermal tumor (PNET) belongs to the PNET/Ewing's sarcoma family. PNET is a small round cell tumor of putative neuroectoderm origin and is the second most common sarcoma among children and young adults. It may occur anywhere in the body and within any age group; however, it is most likely to occur in the bone and soft tissues. There have been a small number of case reports of PNET arising in the ovary. We presented a case of PNET arising in the right ovary of an 18-year-old woman. The tumor was metastased to the lymph nodes of the pelvis and para-aorta at surgical staging. We had persecuted Taxol/carboplatin chemotherapy, pelvic cavity radiotherapy, and Vincristine/Actinomycin, Cyclophosphamide/Doxorubicin (VACA). She died after 10 months due to septic shock.

Adolescent↗
PubMedDate not supplied

Using single-agent therapy in adult patients with advanced soft tissue sarcoma can still be considered standard care.

The group of soft tissue sarcomas in adult patients is a heterogeneous group with more than 40 different subtypes. While local treatment remains the mainstay for localized disease, systemic chemotherapy can importantly contribute in the treatment of advanced soft tissue sarcoma. For patients with metastatic disease, chemotherapy is a palliative treatment in the vast majority of the cases. In this setting, toxicity should not outweigh the potential benefits resulting from chemotherapy. In patients with locally advanced disease too extensive for local treatment, systemic chemotherapy can contribute to cure, provided that tumor shrinkage renders subsequent optimal local treatment possible. In these cases, chemotherapeutic regimens yielding the highest response rates achievable should be used. In the last decades, several randomized studies have aimed to determine whether combination regimens yield benefit over single-agent treatment in terms of response rate and overall survival. This review addresses the current available data on chemotherapy for adult patients with soft tissue sarcoma, excluding gastrointestinal stromal tumor, the Ewing-like sarcomas, and other small blue round cell tumors. In addition, it is increasingly recognized that future research in soft tissue sarcoma should focus on the identification of tumor factors that can serve as targets for treatment and that the diverse tumor subtypes should be analyzed separately for their sensitivity to systemic treatment. This review also focuses on these and other strategies that will hopefully lead to better out comes in this disease entity in the near future.

Adult↗
PubMed2004

Sarcomatoid hepatocellular carcinoma with hepatoblastoma-like features in an adult.

A mixed epithelial and mesenchymal tumor of the liver arising in an adult is rare and is mostly classified as sarcomatoid hepatocellular carcinoma (HCC). In this study, a case of sarcomatoid HCC in an adult with hepatoblastoma (HB)-like features, which produced difficulty in the differential diagnosis between sarcomatoid HCC and mixed HB, is presented. The epithelial component of the tumor composed of poorly differentiated HCC, Edmondson's grade III, and more primitive components, which were embryonal and small cell undifferentiated components of HB-like areas. The small undifferentiated cells surrounded HCC and the embryonal component of HB-like area, and revealed transition partly to areas of rhabdomyosarcoma. A small portion of chondrosarcoma was also noted. Immunohistochemical analysis showed that HCC and the embryonal component of HB-like areas expressed alpha-fetoprotein (AFP) and cytokeratin 8. The small undifferentiated cells were negative for AFP but stained with cytokeratin 8 as well as CD56, which is a marker of primitive cells in many sarcoma and HB. It is not certain whether small undifferentiated cells belong to hepatic progenitor cells or primitive mesenchymal cells. Polymerase chain reaction-single-strand conformation polymorphism analysis for beta-catenin mutation using microdissection revealed no mutation of any components. A review was undertaken of the cases previously reported as adult hepatoblastoma without detailed immunohistochemical study and consider many of them may be sarcomatoid HCC. These primitive and sarcomatoid components would be arising from the dedifferentiation process of HCC.

Aged↗
PubMed2005

Clear cell sarcoma-like tumor with osteoclast-like giant cells in the small bowel: further evidence for a new tumor entity.

Most mesenchymal neoplasms of the gastrointestinal tract belong to the category of gastrointestinal stromal tumors (GISTs) and are characterized by the immunohistochemical expression of KIT receptor. In cases without detectable KIT receptor expression several differential diagnoses have to be taken into consideration. Here, we report a case of a 41-year-old man with a tumor of the small bowel composed of large epithelioid tumor cells arranged in solid and alveolar sheets including scattered osteoclast-like multinucleated giant cells. Immunohistochemically, the tumor cells expressed strongly S-100 protein, vimentin, and to a lesser extent, bcl-2. HMB-45, melan-A, KIT receptor, desmin, smooth-muscle actin, and CD-34 were not detectable. Ki-67 index was 20%. The diagnosis was established by 2 different FISH strategies demostrating the presence of a t(12;22)(q13;q12) translocation, the diagnostic hallmark of clear cell sarcoma of soft parts. Our results provide further evidence for the existence of a new tumor entity designated gastrointestinal clear cell sarcoma with osteoclast-like giant cells. The diagnosis of this entity should be considered in the presence of S-100-positive tumors of the gastrointestinal tract containing multinucleated giant cells and can be established by FISH analysis.

Adult↗
PubMed1995

A new family of genes coding for an antigen recognized by autologous cytolytic T lymphocytes on a human melanoma.

Human melanoma MZ2-MEL expresses several distinct antigens that are recognized by autologous cytolytic T lymphocytes (CTL). Some of these antigens are encoded by genes MAGE-1, MAGE-3, and BAGE, which are expressed in a large fraction of tumors of various histological types but are silent in normal adult tissues with the exception of testis. We report here the identification of the gene coding for MZ2-F, another antigen recognized by autologous CTL on MZ2-MEL cells. This gene, which was named GAGE-1, is not related to any presently known gene. It belongs to a family of genes that are expressed in a variety of tumors but not in normal tissues, except for the testis. Antigenic peptide YRPRPRRY, which is encoded by GAGE-1, is recognized by anti-MZ2-F CTL on class I molecule HLA-Cw6. The two genes of the GAGE family that code for this peptide, namely GAGE-1 and GAGE-2, are expressed in a significant proportion of melanomas (24%), sarcomas (25%), non-small cell lung cancers (19%), head and neck tumors (19%), and bladder tumors (12%). About 50% of melanoma patients carry on their tumor at least one of the presently defined antigens encoded by the MAGE, BAGE, and GAGE genes.

Amino Acid Sequence↗
PubMed1996

Cytogenetics and molecular biology of soft tissue tumors.

Characteristic genetic aberrations have been identified in many soft tissue tumors, and it is likely that several of these aberrations, e.g., the translocation of chromosomes X and 18 in synovial sarcoma, will play an increasing diagnostic role. It is fascinating that most of the consistent soft tissue tumor translocations result in fusion genes, and these fusion genes encode proteins, which in turn regulate the expression of other genes. Thus, many soft tissue tumor translocations represent the first steps in complicated cascades of events contributing to deregulated tumor cell growth. Although a number of translocations appear to be useful in diagnosis, it should be emphasized that cytogenetic and molecular detection of chromosome translocations and gene fusions is not always straightforward. Cytogenetic and molecular analyses are perhaps best reserved for the subgroup of undifferentiated small round cell or spindle cell sarcomas, which remain unclassified after histological, immunohistochemical, and ultrastructural studies. Tumor specimens frozen at -70 degrees C can be used subsequently for FISH and PCR studies, although the opportunity to karyotype such specimens is lost upon freezing.

Chromosome Aberrations↗
PubMed1988

[Contribution of immunology and molecular biology].

Recent technical advances in immunology and molecular genetics have allowed to better delineate Ewing sarcoma among other small round cell tumors of bone and soft tissues. Ewing cells present with a characteristic translocation t (11;22) (q23-24; q11-12) shared with neuroepithelioma. They express a series of cell-surface antigens associated with the neuroectodermal differentiation lineage. These data open new avenues for exploring the origin and the mechanism of transformation of these tumors and to conceive new therapeutical approaches.

Antigens, Surface↗
PubMedDate not supplied

Sarcoma and thyroid disorders: a common etiology?

We have recently observed that many of our sarcoma patients presented also with thyroid disorders. Literature data are almost unavailable on this topic. The relationship between the sarcoma and thyroid disorders is examined. Retrospective analysis of files of patients with sarcoma and clinically overt thyroid disorders was carried out. Of the 375 patients with soft tissue sarcomas (STS) and 235 with bone sarcoma (BS) including small blue round cell tumors (SBRC), 28 patients (4.6%) had an associated significant thyroid disorder. The types of sarcoma were mainly liposarcoma followed by malignant fibrous histiocytoma, leiomyosarcoma and bone sarcoma. The primary sites were mainly limb and trunk. The interval between the diagnosis of the thyroid disorder and the sarcoma varied between -14 years (thyroid first) and +16.5 years (thyroid later) with a median of -0.2 years. Thyroid disorders included goiter, thyroiditis and carcinoma. There are both basic-science and clinical evidence to a possible common pathway that leads to the association between overt thyroid disorders and sarcomas of bone or soft tissues. Oncogene erbA activity is related to thyroid receptors to T3 and to development of sarcoma. Cross talk of the sarcoma oncogene and the erbA might contribute to the development of sarcoma. The thyroid hormone receptor and the highly related viral oncoprotein v-erbA are found exclusively in the nucleus as stable constituents of chromatin. It has been shown that v-erbA can block the spontaneous differentiation in erythroid cells transformed by various retroviral oncogenes. V-erbA can alter the spectrum of neoplasia induced by the v-src oncogene, which causes predominantly sarcomas and erythroblastosis in chicks. The erbA can cooperate with other oncogenes such as v-erbB or with v-fms, v-ras, and c-kit. Cooperation with v-myc may play a role in the development of rhabdomyosarcoma especially in thyroid hormone deficiency state. The possible clinical implications are the need to screen patients with sarcoma to thyroid disorders, and patients with thyroid disorders for malignant diseases.

Adult↗
PubMed1978

A comparison of acridine orange and Feulgen cytochemistry of human tumor cell nuclei.

Specimens of cells derived from tumors of the human female genital tract plus normal cells as standards have been divided into aliquots and stained according to acridine orange or pararosanilin:Feulgen procedures. Acridine orange-stained cells were slit-scanned for 535 nm nuclear fluorescence; Feulgen-stained cells were comb-scanned for 580 nm nuclear absorbance. For each specimen examined, the tumor cell:normal cell ratio of mean nuclear fluorescence following acridine orange staining was greater than the tumor cell:normal cell ratio of mean nuclear absorbance following Feulgen staining. The tumor cell:normal cell ratio of mean nuclear fluorescence ranged from 2.3 for a nonkeratinizing squamous cell carcinoma to 3.9 for a keratinizing squamous cell carcinoma. The tumor cell:normal cell ratio of mean nuclear absorbance ranged from 1.4 for a mixed mesodermal sarcoma to 2.3 for a small cell squamous cell carcinoma. These results indicate that the elevated nuclear fluorescence intensity from acridine orange-stained tumor cells cannot be explained solely on the basis of elevated Feulgen:DNA content. An alternative hypothesis, consistent with these results, is that DNA is the principal binding substrate for intranuclear acridine orange and that the DNA of certain tumor cells is more accessible to acridine orange than is the DNA of normal cells.

Acridines↗
PubMed1993

Analysis of mutant P53 protein in osteosarcomas and other malignant and benign lesions of bone.

Alterations of tumour suppressor genes are considered crucial steps in the development of human cancers. Expressions of p53 protein, a product of the tumour suppressor gene altered most commonly in human cancers examined so far, were investigated immunohistochemically in 18 osteosarcomas and 40 other malignant and benign lesions of bone. A monoclonal antibody clone PAb240, which recognizes a common conformational epitope of mutant p53 proteins, stained nuclei of tumour cells in 12 of 18 osteosarcomas (67%). Six tumours (33%) particularly showed positive immunoreactions in more than half of the tumour cells. PAb240 also stained tumour cells in a small number of other malignant bone tumours, such as malignant fibrous histiocytoma, chondrosarcoma, and Ewing's sarcomas. Furthermore, a small number of cells of giant-cell tumours were positively stained. In contrast, PAb240 was completely negative in 21 benign bone tumours and reactive lesions examined. Another monoclonal antibody clone PAb1801, which reacts with both wild- and mutant-type p53 protein, reacted in nuclei of tumour cells of 7 osteosarcomas (39%). Most of those also reacted with PAb240. PAb1801 was expressed much more frequently in other malignant bone tumours and giant-cell tumours. In addition, PAb1801 showed intranuclear positive reactions in tumour cells of a benign chondroblastoma, and reactive cells such as actively proliferating preosteoblasts in a myositis ossificans and osteoclast-like giant cells in a giant-cell tumour. The immunoelectron-microscopic observation that p53 protein was localized in euchromatic areas of nuclei of osteosarcoma cells supported the specificity of immunoreaction for p53 protein, indicating an active role of p53 protein in the regulation of DNA synthesis and transcription. These findings suggest that point mutation of the p53 gene is frequently involved in the development of osteosarcomas. PAb240 may be a useful tool not only in screening point mutations of the p53 gene in osteosarcomas but also in the differential diagnosis between osteosarcomas and reactive bone-forming lesions. Expressions of mutant p53 protein were not correlated with any clinical or pathological factors examined, although the results should be confirmed in studies of a large number of osteosarcomas.

Adolescent↗
PubMed1995

MIC2 detection in tumors of bone and adjacent soft tissues.

The diagnosis of Ewing's sarcoma has been based classically in large part on the exclusion of other similar small round-cell tumors by light microscopic and histochemical criteria. This study was undertaken to explore the use of a recently developed immunohistochemical stain directed against the glycoprotein p30/32MIC2 antigen (the gene product of MIC2), as a diagnostic tool and as a probe for the examination of potential interrelationships among the putative members of the family of peripheral primitive neuroectodermal tumors. Fifty-six small round-cell tumors of bone were selected for study from the files of the Armed Forces Institute of Pathology and Rhode Island Hospital; all tissues had been formalin fixed and paraffin embedded. Nine of 10 Ewing's sarcomas were MIC2 positive, as were 2 of 3 atypical Ewing's sarcomas (small round-cell tumors that diverged from the classic pattern of Ewing's sarcoma by exhibiting a greater degree of cytologic atypia and pleomorphism), and 7 of 8 Askin tumors of the thoracopulmonary region. Ten of 11 mesenchymal chondrosarcomas, 1 primitive neuroectodermal tumor of bone, 10 small cell osteosarcomas, 10 malignant lymphomas, and 3 sarcomas of bone (not additionally subclassified) were negative. The finding of MIC2 positivity in the majority of Ewing's sarcomas and Askin tumors provides additional support for earlier proposals (based on a shared cytogenetic abnormality, among other criteria) that these lesions be considered members of the same family, the peripheral primitive neuroectodermal tumors. The present study, drawing on archival and current case material (including decalcified and undecalcified specimens), indicates that neither the specimen age nor the application of any of a variety of decalcification solutions appears to adversely influence MIC2 staining of paraffin-embedded tissues. This suggests that this antibody has use in retrospective and prospective studies. The rare occurrence of false negative (in the case of Ewing's sarcoma) and positive results in tumors other than peripheral primitive neuroectodermal tumors (as in 1 of the mesenchymal chondrosarcomas) suggests that MIC2 staining should not be relied on as the sole criterion for identification or exclusion of Ewing's sarcomas and related tumors.

12E7 Antigen↗